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This Article Full Text Full Text (PDF) All Versions of this Article: 92/2/341    most recent expphysiol.2006.036764v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Poole, D. C. Articles by Ferreira, L. F. Search for Related Content PubMed PubMed Citation Articles by Poole, D. C. Articles by Ferreira, L. F. Related Collections Symposia Papers Human, Environmental & Exercise

¹ Department of Kinesiology and Department of Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, USA

Abstract

Sustained performance of muscular exercise is contingent upon increasing muscle O₂ delivery (; the product of blood flow and arterial O₂ content, i.e. ) and utilization () rapidly at exercise onset and sustaining necessary conductive and diffusive O₂ fluxes throughout exercise. A tight co-ordination of pulmonary, cardiovascular and muscle system responses is therefore required to prevent muscle microvascular O₂ pressures (P_mvO2) from falling to levels that impair blood–muscle O₂ exchange and/or impact metabolic control and reduce exercise tolerance. Microvascular O₂ pressures are determined by the balance between and , and emerging evidence indicates that this balance is regulated differently across muscle fibre types and also in aged muscle. Moreover, disease states such as diabetes (type I and II) and chronic heart failure (CHF) also impact P_mvO2. This brief review primarily examines evidence obtained in animals that ageing: (1) redistributes exercising away from highly oxidative muscles and muscle fibres; (2) alters muscle capillary haemodynamics; and (3) reduces the O₂ pressure head within the microcirculation (P_mvO2) that serves to facilitate blood–muscle O₂ transfer. In many respects, these alterations found in healthy ageing animals bear a striking resemblance to those present in some chronic diseases (e.g. diabetes, CHF) and may help explain the compromised exercise tolerance present in aged individuals. Putative mechanistic insights are explored within the context of current knowledge and future investigative approaches.

(Received 13 December 2006; accepted after revision 14 December 2006; first published online 21 December 2006)
Corresponding author D. C. Poole: Department of Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, USA. Email: poole{at}vet.ksu.edu

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				S. A. Ward Muscle-energetic and cardio-pulmonary determinants of exercise tolerance in humans: Muscle-energetic and cardio-pulmonary determinants of exercise tolerance in humans Exp Physiol, March 1, 2007; 92(2): 321 - 322. [Full Text] [PDF]